Research Support, Non-U.S. Gov't
- Lithium Inhibits Growth of Intracellular Mycobacterium kansasii through Enhancement of Macrophage Apoptosis
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Hosung Sohn , Kwangwook Kim , Kil-Soo Lee , Han-Gyu Choi , Kang-In Lee , A-Rum Shin , Jong-Seok Kim , Sung Jae Shin , Chang-Hwa Song , Jeong-Kyu Park , Hwa-Jung Kim
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J. Microbiol. 2014;52(4):299-306. Published online February 17, 2014
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DOI: https://doi.org/10.1007/s12275-014-3469-6
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Abstract
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Mycobacterium kansasii (Mk) is an emerging pathogen that causes a pulmonary disease similar to tuberculosis. Macrophage apoptosis contributes to innate host defense against mycobacterial infection. Recent studies have suggested that
lithium significantly enhances the cytotoxic activity of death stimuli in many cell types. We examined the effect of lithium on the viability of host cells and intracellular Mk in infected macrophages. Lithium treatment resulted in a substantial reduction
in the viability of intracellular Mk in macrophages. Macrophage cell death was significantly enhanced after adding lithium to Mk-infected cells but not after adding to uninfected macrophages. Lithium-enhanced cell death was due to an apoptotic response, as evidenced by augmented DNA fragmentation and caspase activation. Reactive oxygen species were essential for lithium-induced apoptosis. Intracellular
scavenging by N-acetylcysteine abrogated the lithiummediated decrease in intracellular Mk growth as well as apoptosis. These data suggest that lithium is associated with control of intracellular Mk growth through modulation of the apoptotic response in infected macrophages.
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Citations
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